Adherence is an important early event in the pathogenesis of bacterial infections in animals and humans. Studies have shown that the infectious ability of bacteria is related to the ability of bacteria to adhere to host cells. In the first stages of infection, bacterial adhesins, adhesive molecules on the surface of bacteria, bind to receptor materials on the host cell membrane.
Surprisingly, it has been found that the adherence of a bacterium such as Streptococcus pyogenes to human epithelial pharangeal and oral mucosal cells can be inhibited by oligosaccharides. Streptococcus Pyogenes, a group A beta hemolytic streptococci which causes pharyngitis, exhibits tissue tropism, i.e. it is virtually found only in humans.
Early studies by Ellen and Gibbons (Infection and Immunity, pp. 826-830 May 1972) indicated that M protein functions in the attachment of S. pyogenes to epithelial surfaces. On the other hand, subsequent studies by Beachey (J. of Infectious Diseases, 143 (3), pp. 325-345 (1981)) indicated that attachment of S. pyogenes to host receptor cells occurred through fatty acid ends of lipoteichoic acid molecules on the S. pyogenes surface interacting with host cell membrane receptors. More recently Tylewska et al (Current Microbiology, 16, pp. 209-216 (1988)) have confirmed that the M protein in the S. pyogenes cell membrane may play an important role in S. pyogenes adhesion to host cell membranes. While the inventors do not wish to be bound to any one theory, it is believed that inhibition by oligosaccharide of the adherence of S. pyogenes to human pharyngeal and oral mucosal cells may be accomplished by the oligosaccharide effectively mimicing the host cell receptors for M protein, thus preventing binding of S. pyogenes to the receptors of M protein on the host cell membrane.